Hansen Troels Krarup, Thiel Steffen, Knudsen Søren Tang, Gravholt Claus Højbjerg, Christiansen Jens Sandahl, Mogensen Carl Erik, Poulsen Per Løgstrup
Medical Department M, Aarhus University Hospital, Aarhus University, DK-8000 Aarhus, Denmark.
J Clin Endocrinol Metab. 2003 Oct;88(10):4857-61. doi: 10.1210/jc.2003-030742.
The hepatic protein mannan-binding lectin (MBL) activates the complement system on binding to carbohydrate patterns and is involved in first-line defense against invading microorganisms. Emerging evidence indicates that in some situations MBL may cause inexpedient complement activation and tissue injury through binding to endothelial glycosylations. MBL levels are suppressed by insulin treatment in critically ill patients, and, hypothetically, hepatic portal hypoinsulinemia could lead to increased levels of MBL in patients with type 1 diabetes. We measured MBL and C-reactive protein (CRP) levels in 132 normoalbuminuric type 1 diabetic patients and 66 healthy age- and sex-matched controls. The median MBL concentration was higher in diabetic patients than in healthy controls [1290 micro g/liter (interquartile range, IQR 354-2961 micro g/liter) vs. 970 micro g/liter (IQR 277-1607 micro g/liter), P = 0.025], whereas CRP concentrations were similar among patients and controls [1.42 mg/liter (IQR 0.95-2.21) vs. 1.21 mg/l (IQR 0.74-2.13), NS]. In diabetic subjects, CRP levels correlated with poor glycemic control as indicated by hemoglobin A(1c) and daily insulin dose, which was not the case with MBL. MBL concentrations were positively correlated with urinary albumin excretion (r = 0.22; P = 0.013) and increased with increasing urinary albumin excretion tertile (P = 0.036). In conclusion, our data demonstrate that circulating MBL concentrations are significantly elevated in patients with type 1 diabetes and suggest a possible role of MBL in the pathogenesis of renovascular complications in diabetes.
肝脏蛋白甘露聚糖结合凝集素（MBL）在与碳水化合物模式结合时激活补体系统，并参与抵御入侵微生物的一线防御。新出现的证据表明，在某些情况下，MBL可能通过与内皮糖基化结合而导致不适当的补体激活和组织损伤。重症患者接受胰岛素治疗后MBL水平会受到抑制，并且据推测，肝门静脉低胰岛素血症可能导致1型糖尿病患者的MBL水平升高。我们测量了132例正常白蛋白尿的1型糖尿病患者和66例年龄及性别匹配的健康对照者的MBL和C反应蛋白（CRP）水平。糖尿病患者的MBL浓度中位数高于健康对照者[1290微克/升（四分位间距，IQR 354 - 2961微克/升）对970微克/升（IQR 277 - 1607微克/升），P = 0.025]，而患者和对照者的CRP浓度相似[1.42毫克/升（IQR 0.95 - 2.21）对1.21毫克/升（IQR 0.74 - 2.13），无显著性差异]。在糖尿病受试者中，CRP水平与糖化血红蛋白A1c和每日胰岛素剂量所表明的血糖控制不佳相关，而MBL并非如此。MBL浓度与尿白蛋白排泄呈正相关（r = 0.22；P = 0.013），并且随着尿白蛋白排泄三分位数的增加而升高（P = 0.036）。总之，我们的数据表明1型糖尿病患者的循环MBL浓度显著升高，并提示MBL在糖尿病肾血管并发症发病机制中可能发挥作用。
